Observations that implicate aromatic amines and not their acetylated metabolites as a cause of systemic lupus erythematosus (SLE) have been made. We plan to definitively evaluate this in man by comparing the rate of development of ANA in patients receiving procainamide with that in patients receiving N-acetylprocainamide. We also plan to study the rate of ANA development in mice fed procainamide, acetylprocainamide, aromatic amines from food dyes including FD and C Red number 2 and its reduction product, naphthionic acid, and N-acetylated naphthionic acid, and hair dye constituents including diaminoanisole and its N-acetylated product to learn if environmental aromatic amines can incite ANA production and learn the structure-activity relationship for this effect. We plan to study both transglutaminase activity in plasma and whole body N-oxidizing activity of patients with idiopathic SLE and compare them to appropriately selected controls to learn if patients with SLE have high activity of these two pathways by which an aromatic amine might be convalently bound to a nuclear macromole making it foreign and antigenic. If either of these pathways are active in SLE, family studies of the patients will be done to evaluate the role of inheritance in the activity of the pathway.